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Cerium Chloride Application Promotes Wound Healing and Cell Proliferation in Human Foreskin Fibroblasts.

ABSTRACT: This study investigated the effect of cerium chloride (CeCl₃) on cell migration and gene expression of human foreskin fibroblasts (HFF). HFF were exposed to three different CeCl₃ solutions (1%, 5% and 10%, w/v %) for three different time durations (1, 5 and 10 min). 72 h after exposure to CeCl₃, cell viability was assessed by MTT test. A scratch-wounded assay determined the cell migration and the width of the wound, measured at 24 h. Gene expression patterns for cyclins B1, D1 and E1 were analyzed by RT-PCR (p < 0.05, t-test). The viability proliferation increased at 1- and 5-min exposures for all CeCl₃ concentrations, in contrast to no treatment (p < 0.05 at 24 h). No influence of CeCl₃ was found after 10 min. The scratch assay showed increased cell migration up to 60% at 1 and 5 min after 24 h at 5% and 10%. Cyclin B1, D1 and E1 all showed upregulation, confirming an increase in cell proliferation. This study demonstrates that exposure time and concentration of CeCl₃ may have a positive effect on fibroblast viability and migration. Application of CeCl₃ may be beneficial as a cell-stimulating agent leading to therapeutic tissue fibrosis or more resistant tissue around teeth, when warranted, during different periodontal therapies.

SUBMITTER: Ramenzoni LL

PROVIDER: S-EPMC5552080 | biostudies-other | 2017 May

REPOSITORIES: biostudies-other

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Project description:This study investigates the effects of environmentally-relevant concentrations of fluoxetine (FLX, commercial name: Prozac) on wound healing. Pollution of water systems with pharmaceutical and care products, including antidepressants such as FLX and other selective serotonin reuptake inhibitors, is a growing environmental concern. Environmentally-relevant FLX concentrations are known to impact physiological functions and behaviour of aquatic animals, however, the effects of exposure on humans are currently unknown. Using a combination of human skin biopsies and keratinocyte cell lines, we show that exposure to environmental FLX enhances wound closure. We show dose-dependent increases in wound closure with FLX concentrations from 125 ng/l. We demonstrate that the mechanisms underlying enhanced wound closure are increased cell proliferation and serotonin signalling. Transcriptomic analysis revealed 350 differentially expressed genes after exposure. Downregulated genes were enriched in pathways related to mitochondrial function and metabolism, while upregulated genes were associated with cell proliferation and tissue morphogenesis. Kinase profiling showed altered phosphorylation of kinases related to the MAPK pathway. Consistent with this, phosphoproteomics analyses identified 235 differentially phosphorylated proteins after exposure, with enriched GO terms related to cell cycle, division, and protein biosynthesis. These findings collectively show that exposure to environmental FLX promotes wound healing through modulation of serotonin signalling, gene expression and protein phosphorylation, leading to enhanced cell proliferation. Our results open the door for further research to investigate the effects of environmental FLX on cell metabolism and proliferation, and clinical applications of FLX in the setting of wound healing. We argue that there is an urgent need to develop models that can inform on the risks, and potential benefits, of environmental pollution with selective serotonin reuptake inhibitors.

Project description:BackgroundDespite progress in developing wound care strategies, there is currently no treatment that promotes the self-tissue repair capabilities. H2 has been shown to effectively protect cells and tissues from oxidative and inflammatory damage. While comprehensive effects and how H2 functions in wound healing remains unknown, especially for the link between H2 and extracellular matrix (ECM) deposition and epidermal stem cells (EpSCs) activation.MethodsHere, we established a cutaneous aseptic wound model and applied a high concentration of H2 (66% H2) in a treatment chamber. Molecular mechanisms and the effects of healing were evaluated by gene functional enrichment analysis, digital spatial profiler analysis, blood perfusion/oxygen detection assay, in vitro tube formation assay, enzyme-linked immunosorbent assay, immunofluorescent staining, non-targeted metabonomic analysis, flow cytometry, transmission electron microscope, and live-cell imaging.ResultsWe revealed that a high concentration of H2 (66% H2) greatly increased the healing rate (3 times higher than the control group) on day 11 post-wounding. The effect was not dependent on O2 or anti-reactive oxygen species functions. Histological and cellular experiments proved the fast re-epithelialization in the H2 group. ECM components early (3 days post-wounding) deposition were found in the H2 group of the proximal wound, especially for the dermal col-I, epidermal col-III, and dermis-epidermis-junction col-XVII. H2 accelerated early autologous EpSCs proliferation (1-2 days in advance) and then differentiation into myoepithelial cells. These epidermal myoepithelial cells could further contribute to ECM deposition. Other beneficial outcomes include sustained moist healing, greater vascularization, less T-helper-1 and T-helper-17 cell-related systemic inflammation, and better tissue remodelling.ConclusionWe have discovered a novel pattern of wound healing induced by molecular hydrogen treatment. This is the first time to reveal the direct link between H2 and ECM deposition and EpSCs activation. These H2-induced multiple advantages in healing may be related to the enhancement of cell viability in various cells and the maintenance of mitochondrial functions at a basic level in the biological processes of life.

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Cerium Chloride Application Promotes Wound Healing and Cell Proliferation in Human Foreskin Fibroblasts.

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